Panminerva medica · 2017
Cardiovascular consequences of hypophosphatemia.
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Ariyoshi Nobuhiro, Nogi Masayuki, Ando Akika, Watanabe Hideaki, Umekawa Sari
Аннотация
INTRODUCTION: Few studies have been conducted to evaluate the effect of hypophosphatemia on cardiovascular consequences. The goal of this review was to determine whether hypophosphatemia is associated with cardiovascular consequences and to increase its awareness as a new clinical entity and a reversible cause of cardiovascular consequences.
EVIDENCE ACQUISITION: We searched MEDLINE and PubMed through September 2016 for primary studies that reported the relationship between hypophosphatemia and cardiovascular consequences including cardiomyopathy and arrhythmia.
EVIDENCE SYNTHESIS: A total of 937 articles were initially obtained. Of these articles, 921 publications were excluded according to the inclusion and exclusion criteria. Sixteen articles were included in this review. These articles included 3 prospective cohort studies, 1 retrospective cohort study, 7 case series or case reports, 2 case-control studies, 1 pre- vs. post-test in a single group, and 2 animal studies.
CONCLUSIONS: The mechanisms of hypophosphatemia in cardiomyopathy and arrhythmia have been reported to be a depletion of adenosine triphosphate in myocardial cells and decreased 2,3-diphosphoglycerate in erythrocytes. Left ventricular performance seems to improve when severe hypophosphatemia is corrected, but not in those with mild to moderate hypophosphatemia. However, analyses of the relationship between cardiac function and hypophosphatemia using clinical end points have not been conducted. The association between hypophosphatemia and arrhythmia remains unclear, but anecdotal reports exist in the literature.
EVIDENCE ACQUISITION: We searched MEDLINE and PubMed through September 2016 for primary studies that reported the relationship between hypophosphatemia and cardiovascular consequences including cardiomyopathy and arrhythmia.
EVIDENCE SYNTHESIS: A total of 937 articles were initially obtained. Of these articles, 921 publications were excluded according to the inclusion and exclusion criteria. Sixteen articles were included in this review. These articles included 3 prospective cohort studies, 1 retrospective cohort study, 7 case series or case reports, 2 case-control studies, 1 pre- vs. post-test in a single group, and 2 animal studies.
CONCLUSIONS: The mechanisms of hypophosphatemia in cardiomyopathy and arrhythmia have been reported to be a depletion of adenosine triphosphate in myocardial cells and decreased 2,3-diphosphoglycerate in erythrocytes. Left ventricular performance seems to improve when severe hypophosphatemia is corrected, but not in those with mild to moderate hypophosphatemia. However, analyses of the relationship between cardiac function and hypophosphatemia using clinical end points have not been conducted. The association between hypophosphatemia and arrhythmia remains unclear, but anecdotal reports exist in the literature.